Aust Gold
The Deleterious Effects of Asbestos Inhalation and Ingestion
The inhalation of asbestos fibers can be deadly depending upon the level and duration of exposure. One interesting article that explores the oxidation of biomolecules is it related to exposure is called, “Iron mobilization from asbestos by chelators and ascorbic acid” by Loren G. Lund and Ann E. Aust – Archives of Biochemistry and Biophysics – Volume 278, Issue 1, April 1990, Pages 60-64. Here is an excerpt: “Abstract – The ability of chelators and ascorbic acid to mobilize iron from crocidolite, amosite, medium- and short-fiber chrysotile, and tremolite was investigated. Ferrozine, a strong Fe(II) chelator, mobilized Fe(II) from crocidolite (6.6 nmol/mg asbestos/h) and amosite (0.4 nmol/mg/h) in 50 m NaCl, pH 7.5. Inclusion of ascorbate increased these rates to 11.4 and 4.9 nmol/mg/h, respectively.
Ferrozine mobilized Fe(II) from medium-fiber chrysotile (0.6 nmol/mg/h) only in the presence of ascorbate. Citrate and ADP mobilized iron (ferrous and/or ferric) from crocidolite at rates of 4.2 and 0.3 nmol/mg/h, respectively, which increased to 4.8 and 1.0 nmol/mg/h in the presence of ascorbate. Since ascorbate alone mobilized iron from crocidolite (0.5 nmol/mg/h), the increase appeared to result from additional chelation by ascorbate. Citrate also mobilized iron from amosite (1.4 nmol/mg/h) and medium-fiber chrysotile (1.6 nmol/mg/ h). Mobilization of iron from asbestos appeared to be a function not only of the chelator, but also of the surface area, crystalline structure, and iron content of the asbestos. These results suggest that iron can be mobilized from asbestos in the cell by low-molecular-weight chelators. If this occurs, it may have deleterious effects since this could result in deregulation of normal iron metabolism by proteins within the cell resulting in iron-catalyzed oxidation of biomolecules.”
Another interesting study is called, “Subpleural fat pads in patients exposed to asbestos: distinction from non-calcified pleural plaques.” By E N Sargent, W D Boswell, Jr, P W Ralls and A Markovitz - August 1984 Radiology, 152, 273-277. Here is an excerpt: “Abstract – Thirty patients with known asbestos dust exposure were studied because of uncertainty as to whether or not the pleural changes observed on the radiographs were due to plaques or subpleural fat. The CT scans confirmed that the changes were due to subpleural fat in 14 cases (48%). Characteristic subpleural fat shadows on radiographs and CT scans are described, and the importance of differentiating fat from plaques for medico-legal reasons is emphasized.”
Another interesting study is called, “Interactions of chrysotile and crocidolite asbestos with red blood cell membranes. Chrysotile binds to sialic acid.” By Brody AR, George G, Hill LH. – Lab Invest. 1983 Oct;49(4):468-75. Here is an excerpt: “Abstract – Chrysotile and crocidolite are commonly used forms of asbestos. Hemolysis has been widely used as a test of membrane injury, and it has been shown previously that chrysotile causes rapid breakdown of red blood cells (RBCs), whereas crocidolite is only weakly hemolytic. A reasonable hypothesis set forth to explain the cytotoxic effects of chrysotile maintains that positively charged chrysotile fibers bind to negatively charged sialic acid residues on RBC membranes causing clustering of membrane proteins and increased cell permeability to Na and K ions. Our studies presented here provide two lines of evidence in direct support of this hypothesis. (a) Morphologic–Ultrastructural techniques showed that both chrysotile and crocidolite asbestos bind to and distort more than 85% of RBCs treated for 15 minutes. The distorting effects of chrysotile, but not crocidolite, were almost totally ablated by pretreating the cells with neuraminidase. In addition, gold-conjugated wheat germ agglutinin was used to label the distribution of sialic acid groups on RBC membranes. Pretreatment of the RBCs with chrysotile, but not crocidolite, reduced the number of gold-conjugated wheat germ agglutinin-labeled sites to less than 30% of the control level. (b) Biochemical–The thiobarbituric acid assay was used to determine the percentage of sialic acid that remained with the cell pellet after neuraminidase and/or asbestos treatment. Asbestos treatment alone caused no release of sialic acid from the cells. Neuraminidase treatment for 3.5 hours removed more than 80% of the sialic acid from cell surfaces. Chrysotile, but not crocidolite, asbestos prevented neuraminidase-mediated removal of sialic acid from RBCs. In addition, x-ray energy spectrometry of freeze-dried cells showed that RBCs distorted by chrysotile, but not by crocidolite, exhibited significant alterations in intracellular Na:K ratios. The morphologic and biochemical data strongly support the hypothesis that chrysotile asbestos binds to sialic acid groups on RBC membranes. Consequently, the sialic acid residues are redistributed on the surfaces of distorted cells which then are unable to maintain a normal Na:K balance with the surrounding medium.”
If you found any of these excerpts interesting, please read the studies in their entirety. We all owe a great debt to these researchers for their important work.
About the Author
Monty Wrobleski is the author of this article on Texas Mesothelioma Attorney,
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